Katsu Funai, PhD
Associate Professor & Associate Chair of Research,
University of Utah
Featured in the Session: Organellar Metabolite Carriers: A New Frontier in Metabolic Research
When
Monday, June 8
at 8:00 a.m. CT
Where
356 (Level 3)
Ernest N. Morial Convention Center
What is your presentation about?
Resistance in the insulin signaling cascade has been implicated as the major driver for diet/obesity-induced reduction in skeletal muscle glucose transport. We recently developed a mouse model of sedentary behavior to demonstrate that physical inactivity also decreases skeletal muscle glucose transport, but the mechanisms for attenuated glucose catabolism appeared to be at the level of mitochondrial pyruvate entry. We are actively exploring the molecular mechanisms by which sedentary behavior alters a number of metabolic pathways to promote diseases.
How do you hope your presentation will impact diabetes research or care?
Incretin mimetics represent a significant breakthrough in the treatment of obesity and related metabolic diseases including diabetes. While dramatic efficacy for diabetes, cardiovascular diseases, and kidney diseases have been reported, a substantial proportion of patients remains in need of additional treatments. This likely highlights the reality that excess energy intake and reduced energy expenditure both contribute to these diseases, and emphasizes a need to more deeply understand risk factors and mechanisms associated with sedentary behavior.
How did you become involved with this area of diabetes research or care?
I am an exercise physiologist with training in metabolic diseases, bioenergetics, and mass spectrometry. My interest in the biology of energy metabolism comes from personal experiences as well as an internal conviction that limited mobility is a critical but underappreciated driver for many complex acquired diseases.